Our major goal is to test the effect of dietary vitamin E on the tumorigenicity of established tumor cell lines. We have shown that the vitamin can decrease the tumorigenicity of transplanted tumor cells. This protection is dependent on the dose of tumor cells as well as the dose of vitamin E. The latter goes through an optimum and loses its protective ability at very elevated levels (5g/kg diet). We have shown that vitamin E enhances the response of murine spleen cells to respond to T cell mitogens: Con A and PHA. The ability to respond to these mitogens is taken as a measure of the potential to protect against tumors by cell mediated immunity. The involvement of the immune system in the protection produced by vitamin E was established by showing that protection was abrogated when the mice were exposed to sublethal irradiation (400R). It has been demonstrated in preliminary studies that vitamin E may enhance the antigenicity of the tumor cell as well as its ability to act as a target. We will explore the relationship of vitamin E, the immune system and tumorigenicity. With the aid of monoclonal antibodies to the tumor associated antigens, we will investigate whether vitamin E can increase the antigen display on the tumor cells, therby rendering it a better antigen and possibly a better target. The ability to act as a target may also reflect a cell's ability to repair membrane damage, specifically by increased membrane phospholipid synthesis (Schlager and Basos). Since our tumor cells are affected by the kind of lipid in the diet this is a problem we wish to investigate.